Staphylococcal enterotoxin A-induced fever is associated with increased circulating levels of cytokines in rabbits

Huang, Wu-Tein; Lin, Mao‐Tsun; Won, Shen‐Jeu

doi:10.1128/iai.65.7.2656-2662.1997

Cited by 39 publications

(8 citation statements)

References 45 publications

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“…A previous report shows that rabbits given TSST-1 plus endotoxin (29), or TSST-1 alone (7), develop hypothermia following a transient fever. A recent study with rabbits injected with SEA alone reveals that the fever response is linked to increased levels of IFN-␥, TNF, IL-1, IL-2, and IL-6 in serum (14). In our murine studies, we did not see a temperature increase with the SEs or TSST-1, with or without LPS.…”

contrasting

confidence: 57%

Correlation of Temperature and Toxicity in Murine Studies of Staphylococcal Enterotoxins and Toxic Shock Syndrome Toxin 1

et al. 1999

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This study describes a quick (<12 h) assay for detecting temperature decreases in BALB/c and C57BL/6 mice injected intraperitoneally (i.p.) with staphylococcal enterotoxin A (SEA), SEB, or SEC3 or toxic shock syndrome toxin 1 and a potentiating dose of lipopolysaccharide (LPS). Toxin-specific antisera effectively neutralized the temperature fluctuations in this model. Orally administered SEA or SEB (50 μg/animal), with or without LPS, did not have an effect on temperature or lethality. Versus wild-type mice, transgenic knockout mice lacking the p55 receptor for tumor necrosis factor (TNF) or gamma interferon were protected against an i.p. challenge of SEA plus LPS. The p75 receptor for TNF and intercellular adhesion molecule 1 have a negligible role in this toxic shock model.

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contrasting

confidence: 57%

Correlation of Temperature and Toxicity in Murine Studies of Staphylococcal Enterotoxins and Toxic Shock Syndrome Toxin 1

et al. 1999

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“…To prevent the changes in P450 content and activity induced by the HPLC fractions, the following antibodies were used: a goat anti‐rabbit IL‐1β (anti‐IL‐1β) polyclonal antibody, and an anti‐human IL‐2 (anti‐IL2), an anti‐human IFN‐γ (anti‐IFN‐γ), an anti‐human IL‐6 (anti‐IL‐6), and an anti‐human Epo (anti‐Epo) monoclonal antibodies. The antibodies against human proteins were used to neutralize the homologous rabbit proteins because of the known inter‐species reactivity of these antibodies (Huang et al ., 1997; Muscettola et al ., 1995). An irrelevant monoclonal antibody (IgG to Pseudomona aeruginosa ) served as control.…”

Section: Methodsmentioning

confidence: 99%

Hypoxia‐induced down‐regulation of CYP1A1/1A2 and up‐regulation of CYP3A6 involves serum mediators

Fradette

Bleau

Pichette

et al. 2002

British J Pharmacology

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1 Acute moderate hypoxia modi®es the catalytic activity and expression of certain isoenzymes of hepatic cytochrome P450 (P450). The aim of this study was to document whether hypoxia a ects hepatic P450 directly or through the release of serum mediators. 2 Rabbits were subjected to a FiO 2 of 8% for 48 h, sacri®ced, and serum and hepatocytes were isolated; hepatocytes from control and rabbits with hypoxia were incubated with serum from control and hypoxic rabbits for 4 and 24 h, and total P450 content, CYP1A1, 1A2 and 3A6 activities and expressions were assessed. Sera were fractionated by size exclusion chromatography and fractions tested for their ability to modify activity and amount of P450, and serum mediators were identi®ed through neutralization experiments. 3 Total serum and fractions with proteins of 15 ± 23 and 65 ± 94 kDa of M r reduced P450 content and expression of CYP1A1, 1A2 and 3A6, as well as CYP1A1, 1A2 and 3A6 mRNA. Total serum and the fraction with 32 ± 44 kDa proteins increased CYP3A6 activity and protein and mRNA. The serum mediators implicated in the decrease in activity and expression of CYP1A1, 1A2 and 3A6 were interferon-g (IFN-g), interleukin-1b (IL-1b) and IL-2. Erythropoietin (Epo) was partly responsible for the increase in P450 content and CYP3A6 expression. 4 In conclusion, acute moderate hypoxia diminishes the activity and expression of CYP1A1, 1A2 and CYP1A1, 1A2 mRNA, and increases CYP3A6 protein, activity and CYP3A6 mRNA. Several mechanisms contribute to these changes in P450, among them the release of cytokines acting as serum mediators.

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“…In addition to lethality as an endpoint for SE or TSST-1 intoxication, temperature is a readily measured parameter of shock-induced illness. Historically, rabbits afford an attractive model for SE-and TSST-1-induced shock with either temperature or lethal endpoints [162,167,168]. Similar to humans with TSS [157], rabbits exposed to TSST-1 or SEB have subsequently heightened levels of LPS in the bloodstream [169,170].…”

Section: Animal Models For Ses and Tsst-1: Necessary Steps Toward A Bmentioning

confidence: 99%

Staphylococcus aureus: The Toxic Presence of a Pathogen Extraordinaire

Larkin¹,

Carman²,

Krakauer³

et al. 2009

CMC

121

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Staphylococcus aureus is a facultative, Gram-positive coccus well known for its disease-causing capabilities. In particular, methicillin and vancomycin resistant strains of S. aureus (MRSA and VRSA, respectively) isolated globally represent daunting medical challenges for the 21(st) Century. This bacterium causes numerous illnesses in humans such as food poisoning, skin infections, osteomyelitis, endocarditis, pneumonia, enterocolitis, toxic shock, and autoimmune disorders. A few of the many virulence factors attributed to S. aureus include antibiotic resistance, capsule, coagulase, lipase, hyaluronidase, protein A, fibronectin-binding protein, and multiple toxins with diverse activities. One family of protein toxins is the staphylococcal enterotoxins (SEs) and related toxic shock syndrome toxin-1 (TSST-1) that act as superantigens. There are more than twenty different SEs described to date with varying amino acid sequences, common conformations, and similar biological effects. By definition, very low (picomolar) concentrations of these superantigenic toxins activate specific T-cell subsets after binding to major histocompatibility complex class II. Activated T-cells vigorously proliferate and release proinflammatory cytokines plus chemokines that can elicit fever, hypotension, and other ailments which include a potentially lethal shock. In vitro and in vivo models are available for studying the SEs and TSST-1, thus providing important tools for understanding modes of action and subsequently countering these toxins via experimental vaccines or therapeutics. This review succinctly presents the pathogenic ways of S. aureus, with a toxic twist. There will be a particular focus upon the biological and biochemical properties of, plus current neutralization strategies targeting, staphylcoccocal superantigens like the SEs and TSST-1.

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Staphylococcal enterotoxin A-induced fever is associated with increased circulating levels of cytokines in rabbits

Cited by 39 publications

References 45 publications

Correlation of Temperature and Toxicity in Murine Studies of Staphylococcal Enterotoxins and Toxic Shock Syndrome Toxin 1

Correlation of Temperature and Toxicity in Murine Studies of Staphylococcal Enterotoxins and Toxic Shock Syndrome Toxin 1

Hypoxia‐induced down‐regulation of CYP1A1/1A2 and up‐regulation of CYP3A6 involves serum mediators

Staphylococcus aureus: The Toxic Presence of a Pathogen Extraordinaire

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